Nasal polyposis and cystic fibrosis(CF): review of the literature.

The aim of this study was to address whether NP might be a predictive factor for severity of CF. The authors collected data from the literature on NP as a unique or associated sign in CF and reviewed the clinical and molecular aspects of CF associated with NP. CF genotypes and clinical severity in NP(+) vs.

Glutathione S-transferases related to P. aeruginosa lung infection in cystic fibrosis children: preliminary study.

Objectives: In cystic fibrosis (CF) children, we investigated the predictive impact of glutathione S-transferases (GST) activity and genotypes P1, M1 and T1, and antioxidant levels on stage-severity of Pseudomonas aeruginosa lung infection.

Methods: GST activity was determined in whole blood by spectrophotometry, and GST genotypes by multiplex PCR RFLP for 36 CF and 9 control children. Levels of glutathione in erythrocyte and vitamins A, E and C in plasma were measured by HPLC.

Novel CFTR mutations in black cystic fibrosis patients.

Cystic fibrosis (CF) is considered as a rare disease in black Africans. In fact, this disease is likely to be underestimated since clinical features consistent with CF diagnosis are often ascribed to environmental factors such as malnutrition. Very little is known about CFTR mutations in affected patients from Central Africa.

Autoantibodies in D-penicillamine-induced myasthenia gravis: a comparison with idiopathic myasthenia and rheumatoid arthritis.

The distribution of autoantibodies was studied in patients with rheumatoid arthritis (RA) treated by D-penicillamine and who developed myasthenia gravis (MG). The anti-human acetylcholine receptor (AChR) antibodies were specifically associated with clinical symptoms of MG without any difference in the pattern of specificities in idiopathic (id-MG) or in induced MG (DPen-MG). Conversely, anti-nuclear antibodies were elevated in DPen-MG sera compared to id-MG sera (P less than 0.

Anti-histone antibodies in schizophrenia and affective disorders.

Sera from 81 psychiatric patients (51 with schizophrenia and 30 with affective disorders) were analyzed using several assays in parallel for the presence of non-organ-specific autoantibodies, namely anti-nuclear antibodies, anti-deoxyribonucleic acid antibodies (native and denatured DNA), anti-histone antibodies, anti-centromere antibodies, and anti-nuclear antigen antibodies. Nine out of the 81 sera studied were positive for the presence of anti-nuclear antibodies. Moreover, in 15 patients, significant titers of anti-histone antibodies were detected.

Specificity of acebutolol-induced antinuclear antibodies.

Treatment with the beta blocker acebutolol may trigger antinuclear antibody (ANA) production. We retrospectively studied 97 sera from 47 patients who developed ANA during acebutolol treatment. Anti-histone and anti-denatured (ss) DNA antibodies were found in 53% and 66% respectively of the sera tested.

[Myasthenia induced by D-penicillamine. Study of immuno-clinical correlations in 23 cases].

Sera from 23 patients with D-penicillamine-induced myasthenia gravis (MG) contained antibodies directed against the human muscle acetylcholine receptor (anti-AChR) in 83% of the cases at the onset of the disease. Twenty-one were patients with rheumatoid arthritis. The anti-AChR antibody titers were comparable to those of sera from ocular MG patients and were related to the presence of clinical signs but not to their severity.

Effect of LPS on the oxidative metabolism of peritoneal and spleen cells from LPS sensitive and resistant mice.

The influence of LPS on peritoneal and spleen cell oxidative metabolism was investigated in LPS sensitive (C57BL/6) and LPS resistant (C3H/HeJ) mice following intraperitoneal or subcutaneous injection, by measurement of chemiluminescent (CL) responses to latex particles. In C57BL/6 mice, LPS induced a marked increase in peritoneal and spleen cell CL responses, regardless of the route of injection. On the 2nd day, the effect of LPS on peritoneal cells could be fully explained by an inflammatory reaction, while on the 4th day it could be related to an "activated state" of peritoneal macrophages.

[Activation of oxidative metabolism of granulocytes and monocytes by IGG-coated platelets from patients with thrombocytopenia].

We have previously shown that monoclonal anti-T cell antibodies bound to their specific targets can trigger the activation of monocyte/macrophage oxidative metabolism through an Fc receptor-mediated interaction. The present study demonstrates that IgG coated platelets from patients with thrombocytopenia-associated diseases can induce a similar respiratory burst activation in polymorphonuclear and mononuclear phagocytes from normal individuals. The intensity of the oxidative reaction as measured by luminol-dependent chemiluminescence is in close correlation with the level of surface-bound IgG molecules as determined by a radioactive anti-immunoglobulin assay.

Monoclonal antibodies against T cell differentiation antigens initiate stimulation of monocyte/macrophage oxidative metabolism.

Within the first minute after incubation with the mouse anti-human T cell orthoclone monoclonal antibodies OKT3, OKT4, and OKT8, and in the absence of complement, human monocytes generate a burst of highly reactive oxygen metabolites as detected by a luminol-dependent photometric chemiluminescence (CL) assay. The kinetics of the CL responses to these antibodies are identical to that induced by OKM1, the monoclonal antibody to human monocytes and granulocytes. With regard to CL response intensities, OKM1 induces the maximal response and those of OKT3, OKT4, and OKT8 closely reflect the proportion of T cell subsets recognized by these antibodies in peripheral blood.

Modulation of human granulocyte and monocyte chemiluminescence responses: evidence for distinct free radical generating systems.

Using a previously described luminol-dependent photometric chemiluminescence (CL) assay we have investigated the relative significance of the free radicals in the CL phenomenon associated with the respiratory burst of granulocytes and monocytes. The O-2 scavenger, superoxide dismutase, quenches approximately 50% of CL emission from resting and stimulated cells of both types. CL production from granulocytes and monocytes, in the presence of catalase, indicates that H2O2 plays a much less significant role in monocyte light emission than in that of granulocytes.

Chemiluminescence in microamounts of whole blood for investigation of the human phagocyte oxidative metabolism function.

The present study was undertaken in order to investigate more precisely the chemiluminescence (CL) phenomenon and thus the generation of oxygen-free radical products by polymorphonuclear granulocytes (PMN) and monocytes (MN) as takes place in whole blood. A luminol-dependent photometric assay previously devised in our laboratory was used to simultaneously evaluate the CL production by resting cells and cells stimulated by a series of particulate and soluble surface-stimulating agents: latex particles, opsonized zymosan, phorbolmyristate acetate and concanavalin A. In order to quantify the overall light-quenching effect of blood on light emission and subsequently to determine the actual CL output by PMN and MN present in whole blood, Pholad luciferin was used as a constant source of light.

Flash detection of anti-H-2 antibodies using chemiluminescence, without complement.

Within the first minute following their exposure to a specific anti-H-2 serum and in the absence of complement, murine spleen cells generate a chemiluminescence phenomenon which is precisely measurable by photometry in the presence of luminol. The reaction lasts approximately 10 to 20 minutes, it also generated by bone marrow and, although weakly, by peritoneal cells. In contrast, thymus cells remain totally unresponsive.